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Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Energy Metabolism Laboratory, 711 Washington Street, Boston, MA 02111-1524 E-mail: Roberts_EM{at}hnrc.tufts.edu
MRC Childhood Nutrition Research Center, Institute of Child Health, University of London, London, United Kingdom
Rockefeller University, New York, NY
Dear Sir:
Stunkard et al (1) reported data on energy intake and energy expenditure in infants born to lean and overweight mothers and concluded that excessive energy intake, rather than low energy expenditure, is the cause of obesity in infants at high risk of excess weight gain. They also suggested that their results specifically refute the results of an earlier study conducted by 2 of us (2), and therefore by implication also a previous collaborative study by Stunkard (3) and work by other groups (4, 5). We take issue with the interpretation of the new study by Stunkard et al (1) on several grounds, in particular because their results are actually consistent with ours, not contradictory.
In particular, Stunkard et al did not study infants becoming overweight. With mean weight-for-length percentiles decreasing from approximately the 50th percentile at 3 mo of age to the 37th percentile at 12 mo in both low-risk infants (born to lean mothers) and high-risk infants (born to overweight mothers), these were infants who became relatively leaner over time, with no significant difference in actual weight gain between groups. This is a critical difference from the original study by Roberts et al (2), in which infants with a wide range of weight gains were included in the high-risk group and in which 2 groups of high-risk subjects could therefore be distinguished: those who became overweight and those who did not. Thus, what Stunkard et al actually found is that high-risk infants who remain lean do not have low energy expenditures, a finding identical to the original observation of Roberts et al (2) in normally growing infants of overweight mothers and a finding also reported by other groups (6, 7). This is an entirely unrelated finding to the original report of Roberts et al (2) that high-risk infants who gain excess weight have low rates of energy expenditure. Thus, far from refuting the findings of Roberts et al (2), Stunkard et al (1) actually provide further supporting evidence for one aspect of the original results. The further observation of Stunkard et al that weight gain is positively associated with energy intake in lean infants is consistent with the previous report by Roberts (8) of excess energy intake (as well as low energy expenditure) in high-risk infants.
Our second concern with the interpretation of the study by Stunkard et al is the implication that either low energy expenditure or high energy intake is the cause of obesity in infancy. Why not both? The concept of one single determinant of energy balance is far too simplistic given the wealth of data from studies in adults showing the capacity of humans for both overeating and reduced energy expenditure (9–11). We suggested previously that both overeating and underexpending may facilitate weight gain in genetically predisposed infants becoming overweight, depending on environmental circumstances (12). This suggestion is also entirely consistent with laboratory studies of genetically obese rodents showing that both overeating and underexpending can facilitate excess weight gain early in life, with overeating being the dominant mechanism if circumstances permit (13, 14). If food is plentiful, young ob/ob mice will overeat and gain weight, but if food intake is controlled, energy expenditure will drop to facilitate weight gain. Given that the OB gene has been identified in humans (15), the same hierarchy of mechanisms likely exists in some infants also. However, conclusive evidence of the usual importance of low energy expenditure in the development of obesity in different groups of infants is needed. Obtaining such information will require more than simple observational studies to account for the possibility that a hypometabolic state may be easily rectified by excess weight gain and the possibility that hypometabolism may occur transiently at different ages in different infants.
Finally, even if Stunkard et al can in the future identify a group of infants who actually become overweight without exhibiting low energy expenditure, and within the same time period as in previous studies (time frame being an important factor because an infant who becomes overweight by 2 y of age may be metabolically different from one who is overweight by 6 mo), would this mean that low energy expenditure is never a cause of excess weight gain in infancy? Or, would it mean that, compared with infants in the studies in which low energy expenditure was identified as a problem, the infants studied by Stunkard et al were genetically different or subject to different environmental constraints? We strongly suggest that the latter possibility is more likely to be correct in view of the supporting data given above and because obesity is much more prevalent today in the United States (therefore being more likely to be precipitated by favorable environmental circumstances) than it was in England 15 y ago when the original cohort of Roberts et al (2) was identified.
Scientific progress in this area is clearly needed and will be furthered by careful studies identifying the underlying causes of excess weight gain in individual infants. What will not further scientific progress is the use of observational data from nonobese, slowly growing infants to explain the causes of obesity. We can see several good uses for the new data of Stunkard et al (1) on extremely lean infants, but pronouncing on the causes of obesity is not one of them.
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